Question:
In anaphylaxis, bronchoconstriction is primarily mediated by which of the following inflammatory mediators?
In anaphylaxis, bronchoconstriction is primarily mediated by which of the following inflammatory mediators?
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Remember SRS-A (Slow-Reacting Substance of Anaphylaxis) is composed of LTC4, LTD4, and LTE4. This is why leukotriene receptor antagonists (like Montelukast) are useful in managing asthma.
Updated On: Sep 3, 2026
- Leukotriene C4
- Platelet activating factor
- Thromboxane A2
- Interleukin 4
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The Correct Option is A
Solution and Explanation
Concept:
Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction triggered by the rapid, IgE-mediated degranulation of mast cells and basophils. This releases a cascade of preformed and newly synthesized mediators.
Explanation:
• During anaphylaxis, mast cells release preformed mediators (like histamine and tryptase) and synthesize lipid mediators de novo from arachidonic acid (like prostaglandins and leukotrienes).
• The cysteinyl leukotrienes, specifically Leukotriene C4 (LTC4), Leukotriene D4 (LTD4), and Leukotriene E4 (LTE4), were historically known together as the "Slow-Reacting Substance of Anaphylaxis" (SRS-A).
• These cysteinyl leukotrienes are incredibly potent bronchoconstrictors—thousands of times more potent than histamine. They cause sustained smooth muscle contraction in the airways, increased vascular permeability, and massive mucus hypersecretion, leading to the severe respiratory distress seen in anaphylaxis and severe asthma.
• Option (B), Platelet Activating Factor (PAF), is a potent mediator of shock and vascular leak but is not the primary smooth muscle bronchoconstrictor.
• Option (C), Thromboxane A2, primarily mediates platelet aggregation and vasoconstriction.
• Option (D), Interleukin-4, is a cytokine crucial for driving T-helper 2 (Th2) differentiation and IgE class switching, but it is not a direct acute mediator of smooth muscle bronchoconstriction.
Final answer:
Leukotriene C4 is one of the cysteinyl leukotrienes responsible for the intense and sustained bronchoconstriction characteristic of anaphylaxis.
Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction triggered by the rapid, IgE-mediated degranulation of mast cells and basophils. This releases a cascade of preformed and newly synthesized mediators.
Explanation:
• During anaphylaxis, mast cells release preformed mediators (like histamine and tryptase) and synthesize lipid mediators de novo from arachidonic acid (like prostaglandins and leukotrienes).
• The cysteinyl leukotrienes, specifically Leukotriene C4 (LTC4), Leukotriene D4 (LTD4), and Leukotriene E4 (LTE4), were historically known together as the "Slow-Reacting Substance of Anaphylaxis" (SRS-A).
• These cysteinyl leukotrienes are incredibly potent bronchoconstrictors—thousands of times more potent than histamine. They cause sustained smooth muscle contraction in the airways, increased vascular permeability, and massive mucus hypersecretion, leading to the severe respiratory distress seen in anaphylaxis and severe asthma.
• Option (B), Platelet Activating Factor (PAF), is a potent mediator of shock and vascular leak but is not the primary smooth muscle bronchoconstrictor.
• Option (C), Thromboxane A2, primarily mediates platelet aggregation and vasoconstriction.
• Option (D), Interleukin-4, is a cytokine crucial for driving T-helper 2 (Th2) differentiation and IgE class switching, but it is not a direct acute mediator of smooth muscle bronchoconstriction.
Final answer:
Leukotriene C4 is one of the cysteinyl leukotrienes responsible for the intense and sustained bronchoconstriction characteristic of anaphylaxis.
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